A study of the Gribov-Zwanziger action: from propagators to glueballs

This Ph.D. thesis presents a study of the Gribov-Zwanziger framework: from propagators to glueballs. The chapters 2 and 3 are meant as an introduction and only require a basic knowledge of quantum field theory. Chapter 2 explains the techniques behind algebraic renormalization, which shall be widely used throughout this thesis, while chapter 3 tries to give a pedagogic overview of the Gribov-Zwanziger framework as this is not available yet in the literature. The subsequent chapters contain own research. First in chapter 4, we shall dig a bit deeper in the Gribov-Zwanziger framework, by exploring the BRST symmetry and the KO criterium. Next, in chapter 5 we shall elaborate on the ghost and the gluon propagator in the infrared and present a refined Gribov-Zwanziger action. Further, we present two chapters on the search for physical operators within the (refined) Gribov-Zwanziger framework, chapter 6 and 7. A small chapter 8 is devoted to some values for different glueballs. We end this thesis with the conclusions, chapter 9.Comment: 326 pages, Thesis submitted in fulfillment of the requirements for the degree of Doctor (Ph.D.) in Sciences: Physics, obtained on March 11, 201

Effect of myocyte-fibroblast coupling on the onset of pathological dynamics in a model of ventricular tissue

Managing lethal cardiac arrhythmias is one of the biggest challenges in modern cardiology, and hence it is very important to understand the factors underlying such arrhythmias. While early afterdepolarizations (EAD) of cardiac cells is known to be one such arrhythmogenic factor, the mechanisms underlying the emergence of tissue level arrhythmias from cellular level EADs is not fully understood. Another known arrhythmogenic condition is fibrosis of cardiac tissue that occurs both due to aging and in many types of heart diseases. In this paper we describe the results of a systematic insilico study, using the TNNP model of human cardiac cells and MacCannell model for (myo) fibroblasts, on the possible effects of diffuse fibrosis on arrhythmias occurring via EADs. We find that depending on the resting potential of fibroblasts (VFR), M-F coupling can either increase or decrease the region of parameters showing EADs. Fibrosis increases the probability of occurrence of arrhythmias after a single focal stimulation and this effect increases with the strength of the M-F coupling. While in our simulations, arrhythmias occur due to fibrosis induced ectopic activity, we do not observe any specific fibrotic pattern that promotes the occurrence of these ectopic sources

Global alternans instability and its effect on non-linear wave propagation : dynamical Wenckebach block and self terminating spiral waves

The main mechanism of formation of reentrant cardiac arrhythmias is via formation of waveblocks at heterogeneities of cardiac tissue. We report that heterogeneity and the area of waveblock can extend itself in space and can result formation of new additional sources, or termination of existing sources of arrhythmias. This effect is based on a new form of instability, which we coin as global alternans instability (GAI). GAI is closely related to the so-called (discordant) alternans instability, however its onset is determined by the global properties of the APD-restitution curve and not by its slope. The APD-restitution curve relates the duration of the cardiac pulse (APD) to the time interval between the pulses, and can easily be measured in an experimental or even clinical setting. We formulate the conditions for the onset of GAI, study its manifestation in various 1D and 2D situations and discuss its importance for the onset of cardiac arrhythmias

Modeling the Landau-gauge ghost propagator in 2, 3, and 4 spacetime dimensions

We present an analytic description of numerical results for the ghost propagator G(p(2)) in the minimal Landau gauge on the lattice. The data were produced in the SU(2) case using the largest lattice volumes to date, for d = 2, 3 and 4 spacetime dimensions. Our proposed form for G(p(2)) is derived from the one-loop relation between ghost and gluon propagators, considering a tree-level ghost-gluon vertex and our previously obtained gluon-propagator results [A. Cucchieri et al., Phys. Rev. D 85, 094513 (2012). Although this one-loop expression is not a good description of the data, it leads to a one-parameter fit of our ghost-propagator data with a generally good value of chi(2)/d.o.f., comparable to other fitting forms used in the literature. At the same time, we present a simple parametrization of the difference between the lattice data and the one-loop predictions

BRST-Symmetry Breaking and Bose-Ghost Propagator in Lattice Minimal Landau Gauge

The Bose-ghost propagator has been proposed as a carrier of the confining force in Yang-Mills theories in minimal Landau gauge. We present the first numerical evaluation of this propagator, using lattice simulations for the SU(2) gauge group in the scaling region. Our data are well described by a simple fitting function, which is compatible with an infrared-enhanced Bose-ghost propagator. This function can also be related to a massive gluon propagator in combination with an infrared-free (Faddeev-Popov) ghost propagator. Since the Bose-ghost propagator can be written as the vacuum expectation value of a BRST-exact quantity and should therefore vanish in a BRST-invariant theory, our results provide the first numerical manifestation of BRST-symmetry breaking due to restriction of gauge-configuration space to the Gribov region.Comment: 4 pages, 2 figures, 1 tabl

R-from-T as a common mechanism of arrhythmia initiation in long QT syndromes

Background: Long QT syndromes (LQTS) arise from many genetic and nongenetic causes with certain characteristic ECG features preceding polymorphic ventricular tachyarrhythmias (PVTs). However, how the many molecular causes result in these characteristic ECG patterns and how these patterns are mechanistically linked to the spontaneous initiation of PVT remain poorly understood. Methods: Anatomic human ventricle and simplified tissue models were used to investigate the mechanisms of spontaneous initiation of PVT in LQTS. Results: Spontaneous initiation of PVT was elicited by gradually ramping up I-Ca,I-L to simulate the initial phase of a sympathetic surge or by changing the heart rate, reproducing the different genotype-dependent clinical ECG features. In LQTS type 2 (LQT2) and LQTS type 3 (LQT3), T-wave alternans was observed followed by premature ventricular complexes (PVCs). Compensatory pauses occurred resulting in short-long-short sequences. As I-Ca,I-L increased further, PVT episodes occurred, always preceded by a short-long-short sequence. However, in LQTS type 1 (LQT1), once a PVC occurred, it always immediately led to an episode of PVT. Arrhythmias in LQT2 and LQT3 were bradycardia dependent, whereas those in LQT1 were not. In all 3 genotypes, PVCs always originated spontaneously from the steep repolarization gradient region and manifested on ECG as R-on-T. We call this mechanism R-from-T, to distinguish it from the classic explanation of R-on-T arrhythmogenesis in which an exogenous PVC coincidentally encounters a repolarizing region. In R-from-T, the PVC and the T wave are causally related, where steep repolarization gradients combined with enhanced I-Ca,I-L lead to PVCs emerging from the T wave. Since enhanced I-Ca,I-L was required for R-from-T to occur, suppressing window I-Ca,I-L effectively prevented arrhythmias in all 3 genotypes. Conclusions: Despite the complex molecular causes, these results suggest that R-from-T is likely a common mechanism for PVT initiation in LQTS. Targeting I-Ca,I-L properties, such as suppressing window I-Ca,I-L or preventing excessive I-Ca,I-L increase, could be an effective unified therapy for arrhythmia prevention in LQTS

Effects of early afterdepolarizations on excitation patterns in an accurate model of the human ventricles

Early Afterdepolarizations, EADs, are defined as the reversal of the action potential before completion of the repolarization phase, which can result in ectopic beats. However, the series of mechanisms of EADs leading to these ectopic beats and related cardiac arrhythmias are not well understood. Therefore, we aimed to investigate the influence of this single cell behavior on the whole heart level. For this study we used a modified version of the Ten Tusscher-Panfilov model of human ventricular cells (TP06) which we implemented in a 3D ventricle model including realistic fiber orientations. To increase the likelihood of EAD formation at the single cell level, we reduced the repolarization reserve (RR) by reducing the rapid delayed rectifier Potassium current and raising the L-type Calcium current. Varying these parameters defined a 2D parametric space where different excitation patterns could be classified. Depending on the initial conditions, by either exciting the ventricles with a spiral formation or burst pacing protocol, we found multiple different spatio-temporal excitation patterns. The spiral formation protocol resulted in the categorization of a stable spiral (S), a meandering spiral (MS), a spiral break-up regime (SB), spiral fibrillation type B (B), spiral fibrillation type A (A) and an oscillatory excitation type (O). The last three patterns are a 3D generalization of previously found patterns in 2D. First, the spiral fibrillation type B showed waves determined by a chaotic bi-excitable regime, i.e. mediated by both Sodium and Calcium waves at the same time and in same tissue settings. In the parameter region governed by the B pattern, single cells were able to repolarize completely and different (spiral) waves chaotically burst into each other without finishing a 360 degree rotation. Second, spiral fibrillation type A patterns consisted of multiple small rotating spirals. Single cells failed to repolarize to the resting membrane potential hence prohibiting the Sodium channel gates to recover. Accordingly, we found that Calcium waves mediated these patterns. Third, a further reduction of the RR resulted in a more exotic parameter regime whereby the individual cells behaved independently as oscillators. The patterns arose due to a phase-shift of different oscillators as disconnection of the cells resulted in continuation of the patterns. For all patterns, we computed realistic 9 lead ECGs by including a torso model. The B and A type pattern exposed the behavior of Ventricular Tachycardia (VT). We conclude that EADs at the single cell level can result in different types of cardiac fibrillation at the tissue and 3D ventricle level